Expulsion of the urine collected in the urinary bladder during micturition is accomplished by coordinated bladder contraction. Bladder contraction, similar to all smooth muscles, is directly linked to calcium metabolism. However, urinary bladder smooth muscle is significantly different from other smooth muscle in the metabolism and response to pharmacological agents. The contractile characteristics of bladder smooth muscle are altered in hypertrophy, induced either by obstruction or other disease processes. The objective of this proposal is to study the mechanism which regulate the actomyosin ATPase, the in vitro correlate of contraction. Using contractile proteins isolated from normal and obstructed rabbit urinary bladder, experiments will be performed to test the relationship between myosin phosphorylation and actomyosin ATPase in the presence of thin filament-mediated associated proteins, caldesmon and tropomyosin. Furthermore, we will test the hypothesis that the altered contractility of the bladder muscle following obstruction induced hypertrophy is due to alteration of the regulatory mechanism for the function of the contractile machinery, presence of contractile protein isoforms or both. This basic information is essential for our understanding of the bladder function. A better understanding of the regulation of contraction in normal and hypertrophied bladder will enable us to elucidate the pathogenesis of impaired bladder function and to develop proper treatment.